Allergic disease results in considerable economic loss, hardship, and morbidity to millions of Americans every year. Since the immunoglobulin E (IgE) system is a major factor in allergic disease, understanding basic aspects of its synthesis and control are essential for development of proper methods of treatment. The proposed study will extend and investigate a novel method of suppression of IgE biosynthesis in mice already begun in our laboratory, through treatment of neonatal and adult naive and immunized animals with anti-xi antisera. Resulting IgE suppression will be documented by diminution of serum IgE levels and lack of reaginic response upon allergen immunization. Mechanisms involved in such suppression (i.e. residual anti-xi antisera, suppressor cells, abrogation or inhibition of IgE B cells) as well as the resulting effects of IgE suppression on murine defense mechanisms (i.e. resistance to parasitic infection) will be determined. Such studies should provide newer methods of controlling IgE biosynthesis in the mouse and further our understanding of the biological role of IgE biosynthesis in mammalian systems.